Etiology and Pathophysiology

St. Louis encephalitis is caused by an enveloped, single-stranded, positive-sense ribonucleic acid (RNA) virus of the Flaviviridae subgroup. St. Louis encephalitis virus (SLEV) has a relatively conserved nucleotide sequence.

SLEV is an arbovirus transmitted via a mosquito vector from wild birds to humans. Birds, primarily passerine birds such as finches and sparrows, are the principal hosts of the virus. Vectors include the mosquitoes C pipiens, C tarsalis, and C quinquefasciatus.

Risks factors for clinical SLEV infection include the following:

Individuals older than 70 years have a 10-fold increased risk of clinical illness

Exposure to endemic areas or outdoor activities increases risk

Male sex is a risk factor

Most SLEV infection outbreaks occur in people of low socioeconomic status, which is probably due to less access to heath care and poor environmental control of mosquitoes

Comorbidity with atherosclerosis, heart disease, and hypertension is associated with an increased mortality rate of St. Louis encephalitis

A primary viremia follows reproduction of the SLEV at the site of inoculation. In cases of subclinical SLEV infection, the pathogen is cleared by the reticuloendothelial system (the liver, spleen, and lymph nodes) before invasion of the central nervous system (CNS) can occur.

Continued viral replication gives rise to a secondary viremia. Saturation of the filtering capacity of the reticuloendothelial system enables invasion of the CNS. The probability of CNS infection depends on the efficiency of viral replication at the extraneural sites and the degree of viremia. The virus enters the CNS either through the cerebral capillary endothelial cell/astrocyte complex (the blood-brain barrier) or across fenestrated endothelium in areas of the CNS that do not have the usual blood-brain barrier capacity (ie, choroid plexus). Rarely, SLEV tracts retrograde from a peripheral site (the olfactory nerve) that was infected during the viremia.

Many of the flaviviruses exhibit various types of neurotropism. The specific neurotropic mechanisms in SLEV have not been established.

Focal neuronal degeneration with necrosis occurs, leading to the development of glial nodules. Upon healing, spongiform changes occur. The perivascular inflammatory infiltrates are made up of activated T cells and macrophages.

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Epidemiology

St. Louis encephalitis virus (SLEV) is widely distributed from Canada to Argentina. However, human cases have almost exclusively occurred in the United States, especially in eastern and central states. The infections occur as periodic focal outbreaks of encephalitis in the midwestern, western, and southwestern United States, followed by years of sporadic cases. The annual incidence of 0.003-0.752 cases per 100,000 population. SLEV infections have caused large urban epidemics of encephalitis. Outbreaks occur from August through October; however, where the climate is milder, cases can occur year round. The annual reported SLEV neuroinvasive disease cases fluctuate with periodic epidemics. During the last 5 decades, 10,000 cases were reported, with an average of 102 cases reported annually (range 2-1,967).
[2, 3, 4, 5, 6]

Outbreaks of SLEV infection have occurred in Canada and Mexico. Sporadic cases have occurred in South America and the Caribbean.

SLEV infection is reported more often in males than in females, probably due to more outdoor exposure.

The severity of symptoms of SLEV infection increases with age. Older patients are at greater risk of developing clinical illness (especially those >60 y). The literature has reported that up to 90% of elderly individuals who are infected with SLEV develop clinical illness.

Prognosis

The mortality rate of St. Louis encephalitis is 2-30%. This figure is higher in older patients.
[7]

Of persons who survive St. Louis encephalitis, 20% develop sequelae, including irritability, memory loss, various types of movement disorders, or motor deficits. The medical literature also contains reports of syndrome of inappropriate antidiuretic hormone secretion (SIADH) and hyponatremia in patients with St. Louis encephalitis.
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Contributor Information and Disclosures

Author

Charurut Somboonwit, MD, FACP Associate Professor of Internal Medicine, Division of Infectious Disease and International Medicine, University of South Florida College of Medicine; Clinical Research and Communicable Diseases Director, USF Health and Hillsborough Health Department